Anhedonia is a prominent characteristic of depression and related pathology that is associated with a prolonged course of mood disturbance and treatment resistance. However, the neurobiological mechanisms of anhedonia are poorly understood as few studies have disentangled the specific effects of anhedonia from other co-occurring symptoms. Here, we take a transdiagnostic, dimensional approach to distinguish anhedonia alterations from other internalizing symptoms on intrinsic functional brain circuits.

53 adults with varying degrees of anxiety and/or depression completed resting-state fMRI. Neural networks were identified through independent components analysis. Dual regression was used to characterize within-network functional connectivity alterations associated with individual differences in anhedonia. Modulation of between-network functional connectivity by anhedonia was tested using region-of-interest to region-of-interest correlational analyses.

Anhedonia was associated with visual network hyperconnectivity and expansion of the visual, dorsal attention, and default networks. Additionally, anhedonia was associated with decreased between-network connectivity among default, salience, dorsal attention, somatomotor, and visual networks.

Findings suggest that anhedonia is associated with aberrant connectivity and structural alterations in resting-state networks that contribute to impairments in reward learning, low motivation, and negativity bias characteristic of depression. Results reveal dissociable effects of anhedonia on resting-state network dynamics, characterizing possible neurocircuit mechanisms for intervention.

快感缺乏是抑郁症和相关病理的一个突出特征，与长期的情绪障碍和治疗抵抗有关。然而，对快感缺乏的神经生物学机制知之甚少，因为很少有研究将快感缺乏的具体影响与其他同时发生的症状分开。在这里，我们采用跨诊断的维度方法来区分快感缺失的改变与内在功能性脑回路上的其他内化症状。

53 名患有不同程度焦虑和/或抑郁的成年人完成了静息状态 fMRI。通过独立成分分析确定神经网络。双重回归用于表征与快感缺乏个体差异相关的网络内功能连接变化。使用感兴趣区域到感兴趣区域相关性分析测试了快感缺失对网络间功能连接的调节。

快感缺失与视觉网络的超连接性和视觉、背侧注意力和默认网络的扩展有关。此外，快感缺失与默认、显着性、背侧注意力、躯体运动和视觉网络之间的网络间连接性降低有关。

研究结果表明，快感缺失与静息状态网络中的异常连接和结构改变有关，这些改变会导致奖励学习障碍、低动机和抑郁症的消极偏见特征。结果揭示了快感缺乏对静息状态网络动力学的可分离影响，表征了干预的可能神经回路机制。